Maternal age as a source of variation in the ability of an aphid to produce dispersing forms

Summary Apterous parthenogentic females of the pea aphid,Acyrthosiphon pisum (Harris), begin to produce alate offspring soon after they have been subjected to crowding. Females which were born early in their own parent’s reproductive period respond most strongly to crowding, producing much larger numbers of alatae than their late-born sisters. In contrast, the early-born daughters of most alate females do not produce winged offspring after being crowded. Some of their later-born sisters may produce a few winged individuals, resembling in this respect the late-born daughters of the apterous females. Control of the production of alatae thus begins in the grandparental generation. Risk-spreading by means of differential dispersal becomes a less uncertain venture when local populations can modify their responses to environmental changes by utilizing past as well as present signals from their surroundings.     

Pathophysiology of ischemic skin flaps: differences in xanthine oxidase levels among rats, pigs, and humans

Oxygen-derived free radicals have been implicated in a variety of diseases and pathologic processes, including ischemia reperfusion injury (IRI). Based on experimental work with rat skin-flap models, the enzyme xanthine oxidase (XO) has been proposed as a major source of free radicals responsible for tissue injury and flap necrosis. The presence of this enzyme is variable within different tissues of a specific species and between species. Xanthine oxidase levels in pig and human skin have not previously been reported. The activity of xanthine oxidase in the skin of rats (N = 16), pigs (N = 7), and humans (N = 8) was measured after varying intervals of ischemia and in the rat also following reperfusion. Control pig and human skin were found to contain minimal enzyme activity, almost 40 times less than that of the rat. In the rat, xanthine oxidase activity was stable throughout a prolonged period of ischemia, and a significant decrease in activity was found after 12 hours of reperfusion (p less than 0.05). In humans, xanthine oxidase activity was unaffected by ischemia time, and in the pig, it did not increase until 24 hours of ischemia (p less than 0.05). The potential sources of free radicals and the mechanism of action of xanthine oxidase and its inhibitor allopurinol in improving flap survival in different species are reviewed.     

Macrophage activation-associated proteins. Characterization of stimuli and conditions needed for expression of proteins 47b, 71/73, and 120

The expression of cellular proteins was analyzed by two-dimensional gel electrophoresis during and after exposure of mouse macrophages to either mouse rIFN-gamma or natural MuIFN-beta sufficient to prime macrophages for tumor cell killing. The reversible inhibitor of protein synthesis, cycloheximide (CY), was included in some experiments during exposure to IFN. While it was present, CY suppressed protein synthesis by greater than 90%, but did not affect priming for tumor cell killing that was induced by either kind of IFN, as measured in cytotoxicity assays. Further analysis showed that, after CY and IFN were removed, protein synthesis recovered fully within 1 h. p47b, a protein that has been associated closely with the induction of the primed state in mouse macrophages, was then substantially expressed despite no new stimulation by IFN. Thus, macrophages in which protein synthesis had been reversibly inhibited delayed full processing of a signal delivered by IFN, until after protein synthesis had resumed. Such a delay in processing may explain how macrophages subsequently became activated, despite treatment with CY. The expression of the protein doublet, p71/73, was induced, regardless of which of three dissimilar agents (LPS, heat killed Listeria monocytogenes, poly I:C) was used to trigger the expression of cytolytic activity by primed macrophages. Therefore, the likelihood was increased that p71/73, expressed with p47b, is a valid phenotypic marker for fully activated, cytolytic macrophages. By contrast, p120, another protein that has been proposed as a marker of full activation in peritoneal macrophages, was expressed by bone marrow culture-derived macrophages regardless of whether or not they were cytolytic for tumor cells. It cannot be regarded as a reliable marker of macrophage activation in all circumstances, therefore.     

Calls,colours, shape,and genes: a multi‐trait approach to the study of geographic variation in the Amazonian frog Allobates femoralis

Evolutionary divergence in behavioural traits related to mating may represent the initial stage of speciation. Direct selective forces are usually invoked to explain divergence in mate‐recognition traits, often neglecting a role for neutral processes or concomitant differentiation in ecological traits. We adopted a multi‐trait approach to obtain a deeper understanding of the mechanisms behind allopatric divergence in the Amazonian frog, Allobates femoralis. We tested the null hypothesis that geographic distance between populations correlates with genetic and phenotypic divergence, and compared divergence between mate‐recognition (acoustic) and ecological (coloration, body‐shape) traits. We quantified geographic variation in 39 phenotypic traits and a mitochondrial DNA marker among 125 individuals representing eight populations. Geographic variation in acoustic traits was pronounced and tracked the spatial genetic variation, which appeared to be neutral. Thus, the evolution of acoustic traits tracked the shared history of the populations, which is unexpected for pan‐Amazonian taxa or for mate‐recognition traits. Divergence in coloration appeared uncorrelated with genetic distance, and might be partly attributed to local selective pressures, and perhaps to Batesian mimicry. Divergence in body‐shape traits was low. The results obtained depict a complex evolutionary scenario and emphasize the importance of considering multiple traits when disentangling the forces behind allopatric divergence. ©2009 The Linnean Society of London, Biological Journal of the Linnean Society, 2009, 98 , 826–838.     

Nucleotide sequences of Acanthamoeba castellanii 5S and 5.8S ribosomal ribonucleic acids: phylogenetic and comparative structural analyses.

Sequences of 5S and 5.8S rRNAs of the amoeboid protist Acanthamoeba castellanii have been determined by gel sequencing of terminally-labeled RNAs which were partially degraded with chemical reagents or ribonucleases. The sequence of the 5S rRNA is (formula, see text). This sequence is compared to eukaryotic 5S rRNA sequences previously published and fitted to a secondary structure model which incorporates features of several previously proposed models. All reported eukaryotic 5S rRNAs fit this model. The sequence of the 5.8S rRNA is (formula, see text). This sequence does not fit parts of existing secondary structure models for 5.8S rRNA, and we question the significance of such models.     

Wortmannin Reduces Insulin Signaling and Death in Seizure-Prone Pcmt1?/? Mice

L-isoaspartyl (D-aspartyl) O-methyltransferase deficient mice (Pcmt1^−/−) accumulate isomerized aspartyl residues in intracellular proteins until their death due to seizures at approximately 45 days. Previous studies have shown that these mice have constitutively activated insulin signaling in their brains, and that these brains are 20–30% larger than those from age-matched wild-type animals. To determine whether insulin pathway activation and brain enlargement is responsible for the fatal seizures, we administered wortmannin, an inhibitor of the phosphoinositide 3-kinase that catalyzes an early step in the insulin pathway. Oral wortmannin reduced the average brain size in the Pcmt1^−/− animals to within 6% of the wild-type DMSO administered controls, and nearly doubled the lifespan of Pcmt1^−/− at 60% survival of the original population. Immunoblotting revealed significant decreases in phosphorylation of Akt, PDK1, and mTOR in Pcmt1^−/− mice and Akt and PDK1 in wild-type animals upon treatment with wortmannin. These data suggest activation of the insulin pathway and its resulting brain enlargement contributes to the early death of Pcmt1−/− mice, but is not solely responsible for the early death observed in these animals.